<br/>Higher tier endocrine tests like the FSTRA and MEOGRT are used to evaluate the potential for a chemical to cause endocrine disruption in tests.  While variables such as fertility, fecundity, intersex and sex reversal have been identified as apical endpoints, other endpoints are used to evaluate mechanistic outcomes.  Mechanistic endpoints are generally biomarkers that include secondary sex characteristics, vitellogenin, gonad pathology and plasma steroids.  While guidance documents provide performance criteria and statistical methods for the analysis of these variables, there is little guidance on how to integrate all the variables into an overall assessment of whether a chemical is an endocrine disruptor.  Not only is it important to evaluate statistically significant trends, but also whether the magnitude of the responses are statistically significant and biologically relevant relative to controls.  We argue that the pattern of the response is more important than the response of an individual variable.  It is also important that variables are weighted in considering their importance in an overall pattern of responses. Jensen and Ankley (2014) provide guidance on breaking out results into overt toxicity, apical endpoints, and mechanistic endpoints for FSTRA studies, while Borgert et al (2011) have used weight of evidence methodology to evaluate endocrine activity for suites of studies.  We have built on these methodologies to compare responses of known endocrine disruptors to the test chemical in order to identify clear signatures of responses of known ER-agonists, AR-agonists, or AR-antagonists for fish FSTRA and MEOGRT.  Such an approach helps prevent using spurious results to draw erroneous conclusions in evaluating endocrine disruption in fish.<br/>

Improving how we interpret results from the fish short-term reproduction assay (FSTRA) and the medaka extended one generation reproduction Test (MEOGRT)

256th National Meeting (2018)

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